Spinal Mechanisms in Post-Activation Potentiation: Facilitation of Presynaptic Inhibition Contrasts H-Reflex Amplitude Reduction

Abstract

This study investigated the spinal neural mechanisms underlying post-activation potentiation in ten healthy young males (21.9 {+/-} 4.8 years). Participants performed a 10-second maximal isometric plantarflexion, after which we measured twitch torque and assessed spinal excitability using the soleus H-reflex, D1 presynaptic inhibition and heteronymous Ia facilitation (HF). High-density surface EMG was decomposed to track single motor unit responses. The conditioning contraction increased twitch torque by 12.2 Nm (p < 0.001) immediately and returning to baseline within nine minutes. This mechanical potentiation was accompanied by a 29% reduction in H-reflex amplitude (p < 0.001), which recovered within three minutes. Paradoxically, neurophysiological indices of presynaptic inhibition, D1 and HF were significantly increased (D1: p<0.017; HF: p<0.001), resulting in spinal facilitation. Single MU analysis revealed increased discharge probability, particularly in higher-threshold units indicating overall spinal facilitation. These results demonstrate that post-activation potentiation involves a complex dissociation: H-reflex pathway inhibition along with facilitation of presynaptic spinal mechanisms. This paradox can be explained by either post-activation depression (caused by depletion of neurotransmitter at the Ia-motoneuron synapse) or muscle thixotropy, a contraction history-dependent decrease in muscle spindle sensitivity, which reduces the efficacy of the Ia afferent volley independently of spinal inhibitory mechanisms. Our findings highlight a dissociation between spinal presynaptic facilitation and the decreased H-reflex, underscoring the need for future studies to explicitly test the roles of post-activation depression and muscle thixotropy during post-activation potentiation. New & NoteworthyThis study provides evidence that post-activation potentiation reduces the soleus H-reflex amplitude while concurrently facilitating presynaptic spinal mechanisms. By combining global EMG and single motor unit analyses extracted from high-density surface EMG, we reveal a dissociation between spinal disinhibition and reflex depression. These findings suggest that acute post-contraction reflex suppression might be mediated by mechanisms other than presynaptic inhibition, potentially involving post-activation depression spinal mechanisms or changes in muscle spindle sensitivity.